Increased parathyroid cell proliferation and decreased calcium-mediated control of the PTH secretion are characteristic findings in all types of hyperparathyroidism (1-4). Calcium via its receptor, the CaSR and the 1,25(OH)2D-VDR complex are the most important regulators, in this respect. Decreased actions of these regulators would stimulate the parathyroid cells to proliferate. Molecular analyses have revealed the presence of tumor-specific DNA rearrangements in a subset of adenomas. In such rearrangements, the 5' PTH gene regulatory region combines upstream of the Cyclin D1 gene, which results in over expression of cyclins that could induce proliferation by increasing mitotic rate. In fact Cyclin D1 over expression was first demonstrated in a patient with parathyroid adenoma (5).